Exercise performance, haemodynamics, and respiratory pattern do not identify heart failure patients who end exercise with dyspnoea from those with fatigue

Abstract

AimsThe two main symptoms referred by chronic heart failure (HF) patients as the causes of exercise termination during maximal cardiopulmonary exercise testing (CPET) are muscular fatigue and dyspnoea. So far, a physiological explanation why some HF patients end exercise because of dyspnoea and others because of fatigue is not available. We assessed whether patients referring dyspnoea or muscular fatigue may be distinguished by different ventilator or haemodynamic behaviours during exercise.Methods and resultsWe analysed exercise data of 170 consecutive HF patients with reduced left ventricular ejection fraction in stable clinical condition. All patients underwent maximal CPET and a second maximal CPET with measurement of cardiac output by inert gas rebreathing at peak exercise. Thirty‐eight (age 65.0 ± 11.1 years) and 132 (65.1 ± 11.4 years) patients terminated CPET because of dyspnoea and fatigue, respectively. Haemodynamic and cardiorespiratory parameters were the same in fatigue and dyspnoea patients. VO2 was 10.4 ± 3.2 and 10.5 ± 3.3 mL/min/kg at the anaerobic threshold and 15.5 ± 4.8 and 15.4 ± 4.3 at peak, in fatigue and dyspnoea patients, respectively. In fatigue and dyspnoea patients, peak heart rate was 110 ± 22 and 114 ± 22 beats/min, and VE/VCO2 and VO2/work relationship slopes were 31.2 ± 6.8 and 30.6 ± 8.2 and 10.6 ± 4.2 and 11.4 ± 5.5 L/min/W, respectively. Peak cardiac output was 6.68 ± 2.51 and 6.21 ± 2.55 L/min (P = NS for all).ConclusionsIn chronic HF patients in stable clinical condition, fatigue and dyspnoea as reasons of exercise termination do not highlight different ventilatory or haemodynamic patterns during effort.

The Brazilian Society of Cardiology and Brazilian Society of Exercise and Sports Medicine Updated Guidelines for Sports and Exercise Cardiology - 2019

“…Among the additional clinical information that CPET can reveal about athletes or active, healthy individuals, two types stand out: (a) more precise and objective identification of limiting factor(s) for maximum effort (cardiovascular, respiratory and muscular or metabolic) and (b) evaluation of systolic volume behavior, which is obtained by analysis of the curves and maximal values of oxygen pulse (VO 2 /HR) and ventilatory equivalents (VE/VO 2 and VE/VCO 2 ). 62 CPET is already included in cardiological evaluation of HF patients, 63 in identifying the etiology of effort dyspnea 64 , and has more recently been considered capable of identifying myocardial ischemia 65 , 66 or abnormal responses after cardiac surgery. 67 In patients with chest pain, changes in the oxygen pulse during CPET make its diagnostic and predictive accuracy greater than an exercise stress testing for detecting or excluding myocardial ischemia.…”

Cardiac output changes during exercise in heart failure patients: focus on mid‐exercise

“…In our population, rest VO 2 values were lower in HF patients compared with healthy subjects, while they were similar between HF groups; CO and ΔC(a‐v)O 2 were all statistically different between healthy subjects and HF patients, and between Group 1 and Group 2 HF patients. The higher HF patients' ΔC(a‐v)O 2 documented that peripheral mechanism able to increase VO 2 uptake are exploited even at rest in this population of patients 27 . Stroke volume values were significantly higher in healthy subjects compared with HF patients, while the difference between HF patients' values was at threshold for statistical significance ( P = 0.05).…”

From the muscle hypothesis to a muscle solution?

“…If we can improve the failing muscle, we could potentially improve gross muscle function, reduce fatigability, and also, via reducing the action of the overactive muscle ergo‐reflex, potentially reduce sympathetic drive and sympatho‐vagal imbalance. As an aside, similar muscle changes as are seen in HF are also seen in many chronic conditions associated with the risk of cachexia and sarcopenia. If these results hold true for HF, they may also show potential for renal, liver, cancer, and other chronic cachexias and their therapies, thus introducing for the first time a treatment that crosses traditional discipline boundaries more effectively than any to date.…”